Vitamin E deficiency is a very rare problem. It causes neurological problems due to poor nerve conduction. When vitamin E deficiency does occur, it strikes people with diseases that prevent the absorption of dietary fats and fat-soluble nutrients. Since vitamin E is a fat-soluble vitamin, it has some of the properties of fat.

Vitamin E seems to have only one function in the body: the prevention of the natural and continual process of deterioration of all body tissues. This deterioration is provoked by a number of causes; one of these is toxic oxygen. During the body’s metabolism of atmospheric oxygen, toxic oxygen is produced continuously in the body by the formation of by-products. These toxic by-products include hydrogen peroxide, superoxide, and hypochlorite.

Hypochlorite is a natural product, produced by cells of the immune system. It is also the active component of bleach. Once formed, toxic oxygen can damage various parts of the body, such as the membranes which form the boundaries of every cell. Vitamin E serves the body in protecting membranes from toxic oxygen damage. In contrast, vitamin C serves to protect the aqueous, or watery, regions of the cell from toxic oxygen damage. The membranes that are most sensitive to toxic oxygen damage are the membranes of nerves; therefore, the main symptom of vitamin E deficiency is damage to the nervous system.

In developing countries, the most common cause is inadequate intake of vitamin E. In developed countries, the most common causes are disorders that cause fat malabsorption, including cystic fibrosis, pancreatitis, and cholestasis (bile-flow obstruction). Bile salts, produced in the liver, are required for the absorption of fats. Cholestasis causes a decrease in the formation of bile salts and the consequent failure of the body to absorb dietary fats. For this reason, this disease may result in vitamin E deficiency.

Vitamin E deficiency may contribute to retinopathy of prematurity in premature infants and to some cases of intraventricular and subependymal hemorrhage in neonates. Affected premature neonates have muscle weakness.

Another symptom of early vitamin E deficiency in children with cystic fibrosis is a decline in cognitive function, which results in difficulty with reading and falling behind in other intellectual skills during the elementary school years. Researchers have urged the introduction of neonatal screening in order to offset the potential effects of early vitamin E deficiency.

Vitamin E deficiency in humans results in ataxia (poor muscle coordination with shaky movements), decreased sensation to vibration, lack of reflexes, and paralysis of eye muscles. One particularly severe symptom of vitamin E deficiency is the inability to walk.

Attention has been given to the theory that vitamin E serves to protect against cancer and atherosclerosis.